In addition to the contribution made by sympathetically mediated constriction of the capacitance vessels in both exercising and nonexercising parts of the body, venous return is aided by the auxiliary pumping action of the working skeletal muscles and the muscles of respiration (see also ). The intermittently contracting muscles compress the veins that course through them. Because the venous valves are oriented toward the heart, the contracting muscle pumps blood back toward the right atrium (see ). In exercise, the flow of venous blood to the heart is also aided by the deeper and more frequent respirations that increase the pressure gradient between the abdominal and thoracic veins (intrathoracic pressure becomes more negative during exercise).
In humans, blood reservoirs do not contribute much to the circulating blood volume. In fact, blood volume is usually reduced slightly during exercise, as evidenced by a rise in the hematocrit ratio. This decrease in blood volume is caused by water loss externally through sweating and enhanced ventilation and by fluid movement into the contracting muscle. However, fluid loss is counteracted in several ways. Fluid loss from the vascular compartment into the contracting muscles eventually reaches a plateau as interstitial fluid pressure rises and opposes the increased hydrostatic pressure in capillaries of the active muscle. Fluid loss is partially offset by movement of fluid from the splanchnic regions and inactive muscle into the bloodstream. This influx of fluid results from (1) a decrease in hydrostatic pressure in the capillaries of these tissues and (2) an increase in plasma osmolarity because of movement of osmotically active molecules into blood from the contracting muscle. Reduction in urine formation by the kidneys also helps conserve body water.
The large volume of venous blood returning to the heart is so effectively pumped through the lungs and out into the aorta that Pv remains essentially constant. Thus the Frank-Starling mechanism of a greater initial fiber length does not account for the greater stroke volume in moderate exercise. Radiographs of individuals at rest and during exercise reveal a decrease in heart size during exercise. However, during maximal or near-maximal exercise, right atrial pressure and end-diastolic ventricular volume do increase, and the Frank-Starling mechanism contributes to the enhanced stroke volume in very vigorous exercise.
•Fig. 19.18 Cardiacandvascularfunctioncurvesaregreatlyalteredduringstrenuousexercise,whichallowscardiacoutputtoincreasefourfoldtofivefold.TheoperatingpointofthecardiovascularsystemmovesfrompointAtopointB.Thecardiacfunctioncurveduringstrenuousexerciseistheresultofincreasedheartrate,strokevolume,andcontractility.Thevascularfunctioncurvereflectsgreatlydecreasedtotalperipheralresistanceandincreasedmeancirculatorypressure.Atthenewoperatingpoint(pointB),cardiacoutputisincreasedmorethanfourfold,butfillingpressureisincreasedonlyslightly.
In an active, healthy (untrained) individual, the mechanisms previously described typically lead to a fourfold to fivefold increase in cardiac output during vigorous exercise (
Fig. 19.18 ). Increased cardiac output is the fundamental means by which more O2 is delivered to exercising muscles (see
Fig. 19.17 ). The cardiac function curve during exercise reflects increased stroke volume (up to ≈1.5-fold) and heart rate (up to ≈3-fold). The vascular function curve during dynamic exercise reflects a marked decrease in peripheral resistance (changed slope) and an increase in mean circulatory filling pressure (changed intercept), which result from increased venous constriction (tone) in the skeletal muscle “pump,” and the respiratory “pump.” In these conditions, the cardiovascular system is able to operate at a new point (point B in
Fig. 19.18 ), in which cardiac output is increased while filling pressure is little changed. The graphical analysis (see
Fig. 19.18 ) shows that without the systemic changes in vascular function, even a heart beating strongly and fast would be able to produce only a small increase in cardiac output.